Metabolomics reveals disturbed metabolic pathways in human lung epithelial cells exposed to airborne fine particulate matter. Issue 4 (31st March 2015)

• Record Type: Journal Article
• Authors: Huang, Qingyu; Zhang, Jie; Luo, Lianzhong; Wang, Xiaofei; Wang, Xiaoxue; Alamdar, Ambreen; Peng, Siyuan; Liu, Liangpo; Tian, Meiping; Shen, Heqing
• Is Part Of: Toxicology research. Volume 4:Issue 4(2015:Jul.)
• Page Start: 939
• Page End: 947
• Publication Date: 2015-03-31
• Subjects: Toxicology -- Periodicals; 615.9005
• DOI: 10.1039/c5tx00003c
• Languages: English
• ISSNs: 2045-452X

Abstract

Graphical Abstract: Abstract: Exposure to airborne fine particulate matter (PM2.5) has been associated with a variety of adverse health effects; however, the molecular mechanisms involved in PM2.5-elicited pulmonary toxicity are still not well elucidated. By conducting an ultra-high performance liquid chromatography/mass spectrometry-based metabolomics analysis, the present study investigated alterations of metabolome in human lung epithelial cells (A549) exposed to PM2.5 extracts. Distinct metabolomic profiles were found to be associated with PM2.5 treatment. PM2.5 significantly changed the abundance of 16 intracellular metabolites in a dose-dependent manner, of which 13 were decreased and three were increased. By pathway analysis, it was shown that the citrate cycle, amino acid biosynthesis and metabolism, and glutathione metabolism were the major metabolic pathways disturbed by PM2.5 in A549 cells. In addition, changes in expression of several key genes involved in these pathways further validated the metabolic alterations observed by metabolomics herein. It is suggested that PM2.5-induced oxidative stress may contribute to perturbation of metabolic processes occurring in cell mitochondria. Overall, these results aid in improving understanding of the toxicological mechanisms related to PM2.5, and identifying potential biomarkers indicative of inhalable PM2.5 exposure.